Carnitine, the requisite carrier for transmembrane movements of long chain fatty acids, has been shown to reverse long chain acyl CoA ester (LCACAE) inhibition of adenine nucleotide translocase (ANT) activity in vitro. Our recent findings have suggested that oxygen consumption in the ischemic myocardium may be controlled by the limitation of mitochondrial activity through LCACAE inhibition of ANT. In this manner, control of mitochondrial respiration by the electron transport system would be shared with ANT; since myocardial O2 uptake is dependent not only upon the presence of oxygen, but also upon the transport of ADP across the inner mitochondrial membrane. Our working hypothesis suggests that compounds which reverse LCACAE inhibition of ANT should restore mitochondrial function in the ischemic myocardium, if enough oxygen is present to support respiration. This possibility has been strengthened by the demonstration that carnitine partially protected the dog heart myocardium from the ECG and metabolic abnormalities which characterize the early phases of ischemia. Recent studies also indicate that carnitine increases stress tolerance and protects the human ischemic myocardium. The overall effects of carnitine upon the ischemic myocardium are currently under investigation. BIBLIOGRAPHIC REFERENCES: Bittar, N., Shug, A.L., Koke, J.R., Folts, J.D., and Shrago, E.S.: Inhibited adenine nucleotide translocation in mitochondria isolated from ischemic myocardium. In: Recent Advances in Studies on Cardiac Structure and Metabolism, Vol. 7, Biochemistry and Pharmacology of Myocardial Hypertrophy, Hypoxia, and Infarction. Harris, P., Bing, R.J., and Fleckenstein, A., Eds., University Park Press, Baltimore, 1976, pp. 137-143. Sul, H.S., Shrago, E., and Shug, A.L.: Relationship of phosphoenolpyruvate transport, acyl coenzyme A inhibition of adenine nucleotide translocase and calcium ion efflux in guinea pig heart mitochondria. Arch. Biochem. Biophys. 172:230-237, 1976.